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Biomedical subjects

S M Collins

Publications and source records attributed to S M Collins.

At least 199 records · Page 11Linked to original sources
PubMed1983

Sites and mechanisms of action of neuropeptides on canine gastric motility differ in vivo and in vitro.

Motilin, pentagastrin and substance P (SP), injected intra-arterially into the canine gastric corpus in vivo increased the amplitude of contractions by an action dependent on activation of cholinergic nerves; i.e. atropine or tetrodotoxin (TTX) completely blocked the responses to motilin and pentagastrin and increased the ED50 of SP. TTX and atropine were not equally effective in increasing the ED50 for SP in vivo and the effect of combining them depended on the order of their addition. Both were much more effective than the SP analog D-Pro2, D-Trp7,9 SP (DSP) which appeared to be a weak antagonist of actions dependent on neural activity. In strips from the same region in vitro no receptors dependent on cholinergic nerve activation could be demonstrated for any peptide; i.e., all were atropine- and TTX-insensitive. Motilin, as expected in the absence of such receptors caused no contractile response in vitro. SP, also as predicted, caused contractions suggesting that a smooth muscle receptor, independent of nerve activation was present. However contrary to expectation pentagastrin induced an atropine and TTX-insensitive increase in the amplitude and frequency of contractions. These results show that 1) the most sensitive sites of action of a number of excitatory peptides depend on cholinergic nerve function in vivo; 2) such sites or the nerve activity on which they depend cannot be demonstrated in vitro; 3) SP has an additional site of action on smooth muscle demonstrable in vivo and in vitro, but motilin does not; 4) pentagastrin has only an action dependent on nerve function in vivo, but manifests an action independent of nerve function in vitro. We conclude that sites and mechanisms of action of peptides cannot be assumed to be identical in vivo and in vitro. Actions dependent on nerves are often lost in vitro and not all smooth muscle actions can be demonstrated in vivo.

Animals↗
PubMed1983

Quantitative texture analysis in two-dimensional echocardiography: application to the diagnosis of experimental myocardial contusion.

We postulated that the analysis of regional image texture in two-dimensional (2D) echocardiograms would be an accurate method to differentiate normal from abnormal myocardial structure. We tested this hypothesis with quantitative texture measures to study the regional, spatial distribution of echo amplitudes in 2D echocardiograms performed before and immediately after blunt left chest trauma was induced in six anesthetized dogs. After trauma the contused region of myocardium appeared brighter and exhibited an altered myocardial texture. By use of a set quantitative texture measures, we found no significant differences in pretrauma images when normal regions were compared with regions to be contused. Also, we found no difference when we compared the normal regions in each animal in pretrauma vs posttrauma images. Twelve measures, however, differentiated normal from contused regions within the posttrauma images (p values ranged from .0057 to .0001 by multivariate analysis of variance). These texture measures were capable of differentiating normal from abnormal tissue only when texture along the azimuthal (lateral) direction was calculated. We conclude that regions of myocardial contusion exhibit visibly altered local echo-amplitude patterns (altered image texture) and that these image texture alterations may be quantified with digital image analysis techniques. These findings suggest that quantitative texture calculations may be a useful approach to ultrasound tissue characterization.

Animals↗
PubMed1983

Range- and azimuth-dependent variability of image texture in two-dimensional echocardiograms.

Regional two-dimensional (2D) echocardiographic amplitude patterns, or image texture, may be of diagnostic importance. Echocardiographic image texture is due in part to acoustic speckle, a complex pattern of interference of reflections from many small scatterers in tissue. The regional speckle pattern appears to be altered in several disorders associated with abnormalities in myocardial structure but also may be altered by a variety of characteristics of the scanning instrument. We hypothesized that quantitative measures of regional 2D echocardiographic image texture would vary as a function of position in range and azimuth within the field of view, even when imaging a uniform ensemble of scatterers. We tested this hypothesis by imaging a tissue-equivalent phantom with two phased-array scanners and two different methods of digitization. We analyzed the texture in several regions of interest separated in range and azimuth and found significant differences in quantitative texture measures as a function of position of the region of interest in the sector field of view (p values .006 to .0001 by multivariate analysis of variance). We found significant regional variability in texture with both scanners and both methods of digitization. We conclude that regional quantitative image texture in 2D echocardiograms varies as a function of range and azimuth, even when imaging a uniform ensemble of scatterers. This variability is related to several physical and instrument-related phenomena and precludes interpreting all regional texture alterations as indicating tissue structural abnormalities.

Echocardiography↗
PubMed1983

Detection of acute myocardial infarction in closed-chest dogs by analysis of regional two-dimensional echocardiographic gray-level distributions.

We hypothesized that acute myocardial infarction could be detected in standard two-dimensional echocardiograms of closed-chest dogs by evaluating regional echo amplitude distributions using computerized image analysis. We tested this hypothesis by performing standard, 2.4 MHz two-dimensional echoes before and 2 days after circumflex coronary occlusion in seven closed-chest dogs. Control and infarcted regions of interest were studied in digitized stop-frame images. Average gray level was calculated for each region of interest, and the shape of the gray-level distribution was analyzed by calculation of skewness and kurtosis and by qualitative features of shape. Average gray level increased significantly from the pre- to postocclusion images in the infarcted regions (16.7 +/- 4.2 vs. 32.4 +/- 4.4 units, P less than 0.01), but not in the control regions (17.4 +/- 4 vs. 22.3 +/- 5.5., P = NS). Average gray level could not distinguish between infarcted and normal regions within the postocclusion images (36 +/- 5.2 vs. 33.6 +/- 5.8, P = NS). Three independent observers qualitatively evaluated histogram shape and correctly identified 7/7 MI regions (100% sensitivity) and 14/20 normal regions (70% specificity). Quantitatively, infarct regions exhibited a significant decrease in kurtosis from pre- to postocclusion images (7.1 +/- 4.0 vs. 5.2 +/- 2.9, P = NS). Within postocclusion images, infarcted regions displayed a significantly lower kurtosis than did normal regions (0.27 +/- .47 vs. 2.5 +/- 1.0, P less than .01). We conclude that acute myocardial infarction may be detected in closed-chest dogs by analyzing regional echo amplitude data from standard two-dimensional echocardiograms.

Animals↗
PubMed1983

Automatic real-time endocardial edge detection in two-dimensional echocardiography.

Previous approaches to automatic border recognition in two-dimensional echocardiography have utilized off-line computer image analysis. In this paper, we describe a hardware technique for real-time endocardial edge detection during the echocardiographic examination. This technique is based on a new method of line-by-line compensation for ultrasound attenuation. The detected edges and composite edge images can be displayed alone or superimposed upon the usual echocardiographic display. To test the accuracy of our real-time technique, we obtained echocardiograms of excised hearts and compared real-time edges with edges manually traced by an experienced observer. Left ventricular cavity areas and endocardial perimeters derived from real-time edges correlated well with those derived from observer-defined edges.

Echocardiography↗
PubMed1983

Reliability of symptoms in assessing control of gastric acid secretion in patients with Zollinger-Ellison syndrome.

In the present study we explored whether the presence or absence of symptoms could provide a reliable way of assessing the adequacy of control of gastric secretion in patients with Zollinger-Ellison syndrome who were treated medically. Over a 5-yr period, 26 Zollinger-Ellison syndrome patients were entered into a prospective study which examined the presence or absence of symptoms that are associated with gastric hypersecretion, the presence of absence of upper gastrointestinal pathology, and the degree of control of gastric acid secretion. During their last admission, 15 of the 26 patients (58%) were symptomatic, but post-drug gastric acid secretion for the 2 h before the next dose of medication was not significantly different from that in asymptomatic patients. This lack of correlation between the presence or absence of symptoms and post-drug gastric acid secretion was evident for the group as a whole, as well as for 8 to 12 patients who underwent multiple admissions. Of 23 patients who underwent upper gastrointestinal endoscopy of x-ray, or both, on their last admission, 12 had pathology. Post-drug gastric acid secretion was less in patients without pathology than in those with pathology. Furthermore, in patients in whom post-drug gastric acid secretion was less than or equal to 10 mEq/h, the criterion of acceptable control used in this study, pathology did not occur. These findings demonstrate that the presence or absence of symptoms cannot be used to assess the adequacy of medical control of gastric acid secretion in patients with Zollinger-Ellison syndrome. In our opinion, maintenance of post-drug gastric acid secretion less than or equal to 10 mEq/h for the 2 h before the next dose of medication is an acceptable criterion for long-term control of gastric secretion in patients with Zollinger-Ellison syndrome.

Adult↗
PubMed1982

Structural requirements for action of cholecystokinin on enzyme secretion from pancreatic acini.

Using dispersed acini prepared from guinea pig pancreas, we found that the structural requirements for cholecystokinin-induced stimulation of amylase secretion are the same as those for cholecystokinin-induced desensitization of amylase secretion. 1) The relative potencies with which various C-terminal fragments of cholecystokinin cause stimulation are the same as their relative potencies for causing desensitization. 2) With each fragment tested, desensitization occurs with peptide concentrations that are supramaximal for causing stimulation of amylase secretion. 3) Fragments of cholecystokinin less efficacious in causing supramaximal inhibition of amylase secretion are also less efficacious in causing desensitization of amylase secretion. In contrast, there is no obvious fixed relation between the ability of a cholecystokinin fragment to cause stimulation of enzyme secretion and its ability to cause residual stimulation of enzyme secretion. Cholecystokinin and its C-terminal hexadecapeptide are 25-40% more efficacious than the C-terminal decapeptide, octapeptide, and heptapeptide in causing residual stimulation, and the C-terminal pentapeptide and tetrapeptide caused no detectable residual stimulation. The C-terminal tetrapeptide, however, can prevent as well as reverse the residual stimulation caused by other cholecystokinin fragments, and the ability of the tetrapeptide to prevent cholecystokinin-induced residual stimulation is itself fully reversible.

Amylases↗
PubMed1982

Selective modification of the ability of cholecystokinin to cause residual stimulation of pancreatic enzyme secretion.

In the C-terminal heptapeptide of cholecystokinin (-Tyr(SO3H)-Met-Gly-Trp-Met-Asp-Phe-NH2), replacing the aspartic acid residue by beta-aspartic acid did not alter the ability of the peptide to cause stimulation, desensitization, or residual stimulation of enzyme secretion from dispersed pancreatic acini. Replacing the tyrosine sulfate residue by hydroxynorleucine sulfate did not alter the ability of the heptapeptide to cause stimulation or desensitization, but caused a 50-fold decrease in the potency with which the peptide caused residual stimulation of enzyme secretion. These findings suggest that a modification of the N-terminal region of cholecystokinin heptapeptide, which does not alter the ability of the peptide to bind to its receptor on pancreatic acini and by so doing cause stimulation and desensitization of enzyme secretion, can increase the rate at which the bound peptide dissociates when the acini are washed and reincubated. This increased dissociation is reflected by a reduction in the potency with which the peptide causes residual stimulation of enzyme secretion.

Amylases↗
PubMed1982

Cholecystokinin-induced contraction of dispersed smooth muscle cells.

Isolated smooth muscle cells were prepared from the fundus of guinea pig stomach by incubation with collagenase. Incubating the cells with the C-terminal octapeptide of cholecystokinin induced contraction, which was measured by micrometry and expressed as percent decrease in mean cell length. Cholecystokinin-induced contraction was maximal within 30 s and reduced cell length by approximately 37%. The threshold concentration of cholecystokinin was 0.1 pM, and the maximally effective concentration was 0.3 nM. Contraction caused by cholecystokinin could be inhibited by proglumide and by glucagon. Inhibition by proglumide was competitive and resulted in a parallel rightward shift of the cholecystokinin dose-response curve. In contrast, inhibition by glucagon was noncompetitive and resulted in a reduction in the efficacy of cholecystokinin without a change in its potency. Furthermore, proglumide-induced inhibition was specific for cholecystokinin, whereas glucagon-induced inhibition of contraction was nonspecific and reduced the contraction caused by carbamylcholine and the calcium ionophore A23187.

Animals↗
PubMed1981

Nursing--the next 100 years.

This paper sets the scene for future patterns of nursing and nursing education and traces the ways in which the nursing profession has reached the present position. It illustrates the development of nursing over the past 100 years, and examines the key influences which have affected, and are likely to continue to affect, nursing, namely: the Government, the Law and the State; wars and disasters; scientific and technological advances; and people. No attempt has been made to predict or to crystal-gaze, yet the emphasis is firmly placed on the need to plan, to think and to recognize the trends that may determine the future of nursing. Research and education are seen as the tools that will enable nurses to adapt their function to the changing needs of society, whilst preserving the essential or central role of caring. The tapestry--the pattern or web of social relationships, that formed the professional nurse in the Victorian and Edwardian eras, and in the first and second World Wars--presents an unfinished canvas. The present generation of nurses are responsible for continuing to develop that tapestry for future decades, within the framework of the changing social scene of the present day.

Education, Nursing↗
PubMed1981

Initiation of migrating myoelectric complexes in human subjects: role of duodenal acidification and plasma motilin.

The hypothesis that acid, emptied intermittently from the stomach during fasting, might initiate the duodenal phase of the migrating motor complex was tested in normal human subjects. In addition, the relationship between plasma motilin concentrations and the initiation of migrating motor complexes was examined. Migrating complexes occurred spontaneously in the absence of acid in the duodenal bulb and in the presence of duodenal bulb neutralization with sodium bicarbonate. Thus duodenal bulb acidification is not necessary for initiation of the duodenal phase of the migrating motor complexes. Furthermore, cyclical increases in plasma motilin concentrations were not closely correlated with the initiation of the gastric phase of maximal activity of the migrating motor complexes. However, motilin concentrations were decreased significantly following onset of the duodenal phase III. We conclude that neither duodenal acidification nor increases in motilin concentration are necessary to initiate migrating motor complexes in man.

Adult↗
PubMed1981

Changes in plasma motilin concentration in response to manipulation of intragastric and intraduoduenal contents in man.

Immunoreactive plasma motilin concentrations were studied following a variety of stimuli in 24 healthy fasting subjects. Plasma motilin was measured by a radioimmunoassay using antibody GP 71 (J. C. Brown) and natural porcine motilin as standard. Basal motilin levels ranged from undetectable to 365 pg/mL. Antral and intraduodenal infusion of 50 mL o.1 N HCl (pH 1.2) at 5 mL/min failed to alter significantly plasma motilin levels but duodenal acid infusions at 17 mL/min caused a significant increase (70.8 +/- 29.5 pg/mL, mean +/- SEM; n = 6), maximal at 40 min. Duodenal alkalinization with 50 mL 0.3 M Tris buffer (pH 8.0) infused at 5 mL/min produced no change in plasma motilin. A mixed meal did not affect plasma motilin levels. Ingestion of 60 g fat significantly increased plasma motilin (n = 13; maximal increase 150.3 +/- 43.3 pg/mL at 30 min) but duodenal infusions of fat failed to increase plasma motilin levels. These results suggest that motilin secretion induced by fat requires that the fat be present initially within the stomach for secretion to occur. We conclude that ingested fat is a potent stimulus of motilin release. As duodenal acidification (50 mL 0.1 N HCl over 10 min) induces duodenal activity resembling migrating motor complexes but does not release motilin, our data argue against the release of motilin following duodenal acidification as a trigger for the initiation of these complexes in man.

Adult↗
PubMed1981

Cholecystokinin-induced persistent stimulation of enzyme secretion from pancreatic acini.

When pancreatic acini are first incubated with cholecystokinin, washed to remove free cholecystokinin and then reincubated in fresh incubation solution, there is significant residual stimulation of amylase secretion. This residual stimulation requires relatively high concentrations of the secretagogue, is reversible, and is specific for cholecystokinin. Induction of residual stimulation occurs more rapidly at 37 degrees C (maximal by 1 min) than at 4 degrees C (maximal by 10 min), and, once induced, residual stimulation persists for up to 75 min at 37 degrees C and for more than 90 min at 4 degrees C. The persistent effect of cholecystokinin on enzyme secretion cannot be accounted for by incomplete removal of the secretagogue by the wash procedure or by activation of some intermediate step in the mechanism of action of cholecystokinin that persists after the secretagogue dissociates from its receptors. Instead, cholecystokinin-induced residual stimulation of enzyme secretion appears to result from persistent occupation of cholecystokinin receptors by the secretagogue.

Amylases↗
PubMed1981

Reversal of cholecystokinin-induced persistent stimulation of pancreatic enzyme secretion by dibutyryl cyclic GMP.

When pancreatic acini are first incubated with cholecystokinin, washed to remove free cholecystokinin, and then reincubated in fresh incubation solution, there is a significant residual stimulation of amylase secretion. Butyryl derivatives of cyclic GMP can prevent as well as reverse this cholecystokinin-induced residual stimulation. At 37 degrees C the nucleotide-induced reversal is complete within a few minutes, but at 4 degrees C complete reversal requires 90 min of incubation. The ability of butyryl cyclic GMP to reverse cholecystokinin-induced residual stimulation is itself fully reversible, and the nucleotide-induced reversal is accompanied by restoration of full responsiveness to cholecystokinin. The ability of dibutyryl cyclic GMP to reverse cholecystokinin-induced residual stimulation appears to result from the ability of the nucleotide to displace cholecystokinin from its receptors in pancreatic acini.

Amylases↗